Allele Dmel\hop²

General Information
Symbol	Dmel\hop²	Species	D. melanogaster
Name		FlyBase ID	FBal0005513
Feature type	allele	Associated gene	Dmel\hop
Also Known As	hop^C111

Allele class	loss of function allele, amorphic allele - genetic evidence
Mutagen	X ray
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Perrimon and Mahowald, 1986, Hanratty and Dearolf, 1993) loss of function allele (Binari and Perrimon, 1994)
Mutagen	X ray (Binari and Perrimon, 1994)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Deletion of about 300bp of genomic DNA. (Binari and Perrimon, 1994)
Cytology
Phenotypic Data
Phenotypic Class
	cell shape defective \| extended germ band stage \| germline clone (Bertet et al., 2009) lethal \| dominant \| larval stage (Binari and Perrimon, 1994) lethal \| embryonic stage \| recessive \| rescuable maternal effect (Hou et al., 1996) lethal \| recessive (Luo et al., 1995) lethal \| rescuable maternal effect (Perrimon and Mahowald, 1986) planar polarity defective \| cell autonomous \| somatic clone (Luo et al., 1999) planar polarity defective \| cell non-autonomous \| recessive \| somatic clone (Zeidler et al., 1999) planar polarity defective \| cell non-autonomous \| somatic clone (Luo et al., 1999)
Phenotype Manifest In
	abdominal 4 ventral denticle belt (Harrison et al., 1998) abdominal 4 ventral denticle belt \| germline clone \| maternal effect (Chen et al., 2003) abdominal 5 ventral denticle belt (Harrison et al., 1998) abdominal 5 ventral denticle belt \| germline clone \| maternal effect (Chen et al., 2003) abdominal 6 ventral denticle belt (Harrison et al., 1998) abdominal 7 ventral denticle belt (Harrison et al., 1998) abdominal 8 ventral denticle belt (Harrison et al., 1998) border follicle cell (Silver and Montell, 2001) border follicle cell (with hop²⁵) (Xi et al., 2003) border follicle cell \| somatic clone (Xi et al., 2003, Beccari et al., 2002) centripetally migrating follicle cell (with hop²⁵) (Xi et al., 2003) denticle belt \| germline clone \| rescuable maternal effect (Chen et al., 2003) dorsal trunk primordium \| germline clone \| maternal effect (Chen et al., 2003) ectoderm \| extended germ band stage \| germline clone (Bertet et al., 2009) embryonic/larval proventriculus (Josten et al., 2004) embryonic abdominal segment 4 (Hou et al., 1996) embryonic abdominal segment 4 \| non-rescuable maternal effect (Chen et al., 2002) embryonic abdominal segment 5 (Hou et al., 1996) embryonic abdominal segment 5 \| non-rescuable maternal effect (Chen et al., 2002) embryonic head (Hou et al., 1996) embryonic hindgut \| germline clone (Johansen et al., 2003) eye \| somatic clone (Zeidler et al., 1999, Luo et al., 1999) eye equator \| ectopic (Luo et al., 1999) eye photoreceptor cell \| somatic clone (Luo et al., 1999) follicle cell \| posterior (with hop²⁵) (Xi et al., 2003) gonad \| maternal effect (Li et al., 2003) male germline stem cell (Tulina and Matunis, 2001) mesothoracic ventral denticle belt (Harrison et al., 1998) nurse follicle cell (with hop²⁵) (Xi et al., 2003) nurse follicle cell \| somatic clone (Xi et al., 2003, Beccari et al., 2002) ommatidium \| cell non-autonomous \| somatic clone (Zeidler et al., 1999) ommatidium \| somatic clone (Luo et al., 1999) oocyte associated follicle cell (with hop²⁵) (Xi et al., 2003) pole cell \| maternal effect (Li et al., 2003) presumptive embryonic/larval tracheal system (Chen et al., 2002) spermatogonium (Tulina and Matunis, 2001) telson (Hou et al., 1996) testis (Tulina and Matunis, 2001) tracheal branch primordium \| germline clone \| maternal effect (Chen et al., 2003)
Detailed Description
	Statement Reference 40% of embryos from hop[2] germ line clones show germ-band extension defects. Hemizygous hop[2] mutant germ-band epithelial cells are normal in the head and dorsal-most regions of the embryo, however intercalating (ventrolateral) cells show a smaller apical cell surface. (Bertet et al., 2009) The proventriculus development is normal in early stages of proventriculus development in mutants. However in the keyhole stage, the anterior boundary cells fail to move inward into the endodermal keyhole domain and arrest anterior to the proventricular endoderm until late stages of embryonic development. Furthermore, the endodermal cell layer of the keyhole is disorganised and the proventriculus is collapsed. (Josten et al., 2004) Paternally rescued hop² germ-line clone embryos are missing denticle belt A5 and part of A4. In the absence of paternal rescue, more severe segmentation defects are seen. Paternally rescued hop² germ-line clone embryos have defective tracheal systems, generally having several disruptions in the main trunk and several branches. (Chen et al., 2003) Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic hop function) have incompletely elongated hindguts which are wider than normal. There are a greater number of cells in the circumference of the mutant hindgut than in wild type. The total number of hindgut epithelial cells is 89% of wild type. (Johansen et al., 2003) The number of pole cells in embryos derived from hop² female germ line clones is not different to the number in wild-type embryos. However, in late stage embryos these pole cells fail to coalesce and/or form gonads. (Li et al., 2003) hop²⁵/hop² egg chambers lack border follicle cells and have reduced numbers of stretched (nurse) follicle cells and posterior polar follicle cells, but increased numbers of main body (oocyte) follicle cells. Nurse follicle cell and centripetally migrating follicle cell domains are shifted posteriorly. When presumptive border cells are mutant for hop² they fail to express markers of differentiation, and are delayed in migration. When follicle cells overlying the nurse cells are mutant for hop² they fail to stretch at stage 9 as wild-type nurse follicle cells do, or to express nurse follicle cell markers. (Xi et al., 2003) Homozygous mutant border cells, made as somatic clones, fail to migrate. Occasionally a mutant border cell cluster is displaced quite far from the anterior tip of the egg chamber and is associated with abnormally shaped mutant stretch cells. (Beccari et al., 2002) Paternally rescued embryos derived from females containing homozygous germ-line clones lack abdominal segment 5 and part of abdominal segment 4. These embryos form a defective tracheal system with several disruptions in the main trunk and many branches. (Chen et al., 2002) Mosaic egg chambers which are homozygous for hop² in the germline (but not in the soma) are not fused and all contain 15 nurse cells and one oocyte. (McGregor et al., 2002) When homozygous somatic clones are made in the egg chamber, defects in border cell migration are seen. Whenever the polar cells are mutant, a complete failure in border cell migration is seen. However, in egg chambers in which the germ-line is mutant, no migration defect is seen. Nor are border cell defects seen when large clones are made in the rest of the follicle cell epithelium. In mutant egg chambers outer border cell clusters consist of an average of 2.1 cells, as compared to 6 in wild-type. (Silver and Montell, 2001) Mutant adult testes contain hub cells but lack stem cells and spermatogonia. A few spermatocytes and terminal epithelial cells remain. (Tulina and Matunis, 2001) hop² somatic clones in the eye are rare and have a cell autonomous growth disadvantage when compared to their wildtype twins. They occasionally have missing photoreceptor cells and polarity defects. In the rare larger clones a striking cell non-autonomous effect is seen. Ommatidia at the polar margin of the clones reverse their polarity such that the ommatidia point away rather than toward the equator, thus creating an ectopic equator. When a clone is observed very close to the dorso-ventral midline, the equator was deflected away and formed along the border of the clone. Most of the ommatidia with reversed polarity were composed entirely of wild-type photoreceptor cells. This effect was seen in both dorsal and ventral halves of the eye. (Luo et al., 1999) Homozygous clones in the eye show a regular array of ommatidia which contain the wild-type complement of correctly differentiated and positioned photoreceptor cells within the ommatidia. A large proportion of homozygous clones in the eye result in polarity defects in which ommatidia straddling the polar boundary of the clone show inverted dorsoventral polarity. The phenotype is strongest in larger clones and in clones in which the polar boundary runs parallel to the equator of the eye. Typically, one or two rows of ommatidia are inverted, with the strongest phenotype seen having about five inverted rows. Both totally mutant ommatidia adjacent to the polar boundary of the clone and mosaic ommatidia at the clonal border can assume an inverted fate, and occasionally, an ommatidial cluster immediately outside the clone in which all the photoreceptors are wild type is seen to have inverted polarity. Mutant ommatidia in the centre of the clone and on the equatorial margin of the clone show normal orientation. This phenotype is seen in both adults and third larval instar imaginal discs. (Zeidler et al., 1999) hop² embryos derived from homozygous female germ line clones show loss of the fifth abdominal denticle band and the posterior mid-ventral portion of the fourth band. Variable reduction of the second thoracic and eighth abdominal denticle bands and variable fusion of the sixth and seventh denticle bands is seen. (Harrison et al., 1998) Maternal effect segmentation phenotype is similar to that caused by loss of Stat92E activity during embryogenesis. Both paternally rescued and unrescued embryos show a consistent deletion of the fifth abdominal segment and the posterior midventral portion of the fourth abdominal segment. Additional defects are seen in the head and tail of the unrescued embryos. (Hou et al., 1996) Larval diploid imaginal tissues are reduced in size. Embryos derived from females lacking hop die with characteristic segmentation defects, deletion of the fifth abdominal denticle belt and posterior mid-ventral portion of the fourth abdominal denticle belt. (Binari and Perrimon, 1994) Paternal rescue of the maternal effect. Germline clone analysis demonstrates that embryos have one abdominal segment missing and A4 appears wider than wild type, and partial or complete fusion of T1 and T2. (Perrimon and Mahowald, 1986) larval/pupal lethal
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement Reference hop²/hop[+] is an enhancer of visible phenotype of Scer\GAL4^en-e16E, Socs36E^{Scer\UAS.P\T.cCa} (Callus and Mathey-Prevot, 2002) hop²/hop[+] is an enhancer of visible phenotype of Scer\GAL4^en-e16E, Socs44A^Scer\UAS.cRa (Rawlings et al., 2004)
Suppressor of
Statement Reference hop²/hop[+] is a suppressor \| partially of visible phenotype of os^GMR.PB (Bach et al., 2003) hop²/hop[+] is a suppressor \| partially of visible phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, os^Scer\UAS.cCa (Chen et al., 2002) hop² is a suppressor of melanotic mass phenotype \| heat sensitive phenotype of Scer\GAL4^srp.D.cCa, Scer\GAL80^ts.αTub84B, gcm^{DN.Scer\UAS.T:Rep-en} (Jacques et al., 2009)
Phenotype Manifest In
Suppressed by
Statement Reference hop² has abdominal 4 ventral denticle belt \| germline clone \| maternal effect phenotype, suppressible by Cdk4^hs.PC (Chen et al., 2003) hop² has abdominal 4 ventral denticle belt \| germline clone \| maternal effect phenotype, suppressible by CycE^hs.PO (Chen et al., 2003) hop² has abdominal 5 ventral denticle belt \| germline clone \| maternal effect phenotype, suppressible by Cdk4^hs.PC (Chen et al., 2003) hop² has abdominal 5 ventral denticle belt \| germline clone \| maternal effect phenotype, suppressible by CycE^hs.PO (Chen et al., 2003)
Enhancer of
Statement Reference hop²/hop[+] is an enhancer of wing phenotype of Scer\GAL4^en-e16E, Socs36E^{Scer\UAS.P\T.cCa} (Callus and Mathey-Prevot, 2002) hop²/hop[+] is an enhancer of wing vein \| ectopic phenotype of Scer\GAL4^en-e16E, Socs44A^Scer\UAS.cRa (Rawlings et al., 2004) hop²/hop[+] is an enhancer of wing vein L3 phenotype of Scer\GAL4^en-e16E, Socs44A^Scer\UAS.cRa (Rawlings et al., 2004)
Suppressor of
Statement Reference hop²/hop[+] is a suppressor \| partially of eye phenotype of os^GMR.PB (Bach et al., 2003) hop²/hop[+] is a suppressor \| partially of eye phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, os^Scer\UAS.cCa (Chen et al., 2002) hop²/hop[+] is a suppressor \| partially of ommatidium \| supernumerary phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, os^Scer\UAS.cCa (Chen et al., 2002) hop² is a suppressor of melanotic mass \| heat sensitive phenotype of Scer\GAL4^srp.D.cCa, Scer\GAL80^ts.αTub84B, gcm^{DN.Scer\UAS.T:Rep-en} (Jacques et al., 2009)
NOT Suppressor of
Statement Reference hop²/hop² is a non-suppressor of denticle belt \| maternal effect phenotype of tor^12D (Li et al., 2002, Li et al., 2002)
Other
Statement Reference da², hop²/hop[+] has follicle cell phenotype (Smith et al., 2002) da², hop² has follicle cell phenotype (Smith et al., 2002) Scer\GAL4^en-e16E, Socs36E^{Scer\UAS.P\T.cCa}, hop²/hop[+] has wing vein \| ectopic phenotype (Callus and Mathey-Prevot, 2002) Scer\GAL4^en-e16E, Socs36E^{Scer\UAS.P\T.cCa}, hop² has wing vein \| ectopic phenotype (Callus and Mathey-Prevot, 2002)
Additional Comments
Genetic Interactions
Statement Reference The melanotic tumour phenotype caused by expression of gcm[DN.Scer\UAS.T:en-Rep] under the control of Scer\GAL4[srp.D.cCa] (the animals also carry Scer\GAL80[ts.αTub84B] which has been inactivated by shifting to the restrictive temperature) is completely suppressed in a hop[2]/Y background. (Jacques et al., 2009) The ectopic wing vein and arching of wing vein L3 phenotypes caused by expression of Socs44A[Scer\UAS.cRa] under the control of Scer\GAL4[en-e16E] are enhanced by hop[2]/+. (Rawlings et al., 2004) The enlarged eye phenotype seen in flies carrying one copy of os^GMR.PB is moderately suppressed by one copy of hop². (Bach et al., 2003) The loss of denticle belt A5 and gap in denticle belt A4 seen in hop² germ-line clone embryos is suppressed by Cdk4^hs.PC, or CycE^hs.PO, although in both cases the two rescued denticle belts tend to fuse with each other laterally. (Chen et al., 2003) Expression of Socs36E^{Act5C.T:Ivir\HA1} under the control of Scer\GAL4^en-e16E in a hop²/+ background induces ectopic vein formation in 17-26% of wings and the size and penetrance of the humeral outgrowth phenotype is increased. (Callus and Mathey-Prevot, 2002) The extra number of ommatidia caused by expression of os^Scer\UAS.cCa under the control of Scer\GAL4^GMR.PF is partially suppressed by hop²/+; the flies have an average of 854 +/- 9 ommatidia. (Chen et al., 2002)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	hop² is rescued by hop^Scer\UAS.cHa/Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} (Bertet et al., 2009) hop² is rescued by hop^T-r7.Act5C (Luo et al., 1995)
Comments	Expression of hop[Scer\UAS.cHa] under the control of Scer\GAL4[mat.αTub67C.T:Hsim\VP16] rescues the germ-band extension and apical cell shape defects observed in hop[2] germ-line clones. (Bertet et al., 2009)
Stocks ( 2 )
Bloomington	6032 hop²/FM7a
Kyoto	108563 hop²/FM7a
Notes on Origin
Discoverer	Lefevre. G. Lefevre.

Comments
	Fail to complement hop²⁵. (Perrimon and Mahowald, 1986)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 7 )
Reported As
Symbol Synonym	C111 (Chen et al., 2002) hop² (Popodi et al., 2010-, Jacques et al., 2009) hop^C111 (Baeg et al., 2005, Callus and Mathey-Prevot, 2002, Li et al., 2003, Josten et al., 2004, Li et al., 2003, Bach et al., 2003, Chen et al., 2003, Johansen et al., 2003, Ghiglione et al., 2002, Li et al., 2002, Beccari et al., 2002, Silver and Montell, 2001, Luo et al., 1999, Hou et al., 1996, Binari and Perrimon, 1994, Hanratty and Dearolf, 1993, Watson et al., 1991, Bertet et al., 2009, Sotillos et al., 2010) hop^c111 (Xi et al., 2003, Rennebeck et al., 2002, McGregor et al., 2002, Silver and Montell, 2001, Harrison et al., 1998, Rawlings et al., 2004, Almudi et al., 2009) hop^CIII (Luo et al., 1995) l(1)C111 l(1)hop^C111 (Perrimon and Mahowald, 1986)
Name Synonym
Secondary FlyBase IDs

References ( 35 )

Generate a list of	All references relating to this allele ( 35 )

List References by type	Research paper ( 33 ) Personal communication to FlyBase ( 1 ) Abstract ( 1 )
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Allele Dmel\hop2

Allele Dmel\hop²